ArticleCardiovascular research2011
A novel catestatin-induced antiadrenergic mechanism triggered by the endothelial PI3K-eNOS pathway in the myocardium.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- The role of chromogranin A cleavage products in onset of type 1 and 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026Review
- Catestatin in Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- The physiological anti-hypertensive peptide catestatin and its common human variant Gly364Ser: differential cardiovascular effects in a rat model of hypertension.Bioscience reports · 2024Article
- The Role of Catestatin in Preeclampsia.International journal of molecular sciences · 2024Review
- Chromogranin A and its derived peptides: potential regulators of cholesterol homeostasis.Cellular and molecular life sciences : CMLS · 2023Review
- Role of Catestatin in the Cardiovascular System and Metabolic Disorders.Frontiers in cardiovascular medicine · 2022Review
- Sympathetic nervous system activation and heart failure: Current state of evidence and the pathophysiology in the light of novel biomarkers.World journal of cardiology · 2020Review
- Chromogranin A and its fragments in cardiovascular, immunometabolic, and cancer regulation.Annals of the New York Academy of Sciences · 2019Review
- Catestatin Induces Glucose Uptake and GLUT4 Trafficking in Adult Rat Cardiomyocytes.BioMed research international · 2018Article
- Chromogranins: from discovery to current times.Pflugers Archiv : European journal of physiology · 2018Review
- Obestatin regulates cardiovascular function and promotes cardioprotection through the nitric oxide pathway.Journal of cellular and molecular medicine · 2017Article
- Chromogranin A Regulation of Obesity and Peripheral Insulin Sensitivity.Frontiers in endocrinology · 2017Review
- Catestatin Gly364Ser Variant Alters Systemic Blood Pressure and the Risk for Hypertension in Human Populations via Endothelial Nitric Oxide Pathway.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Catestatin attenuates endoplasmic reticulum induced cell apoptosis by activation type 2 muscarinic acetylcholine receptor in cardiac ischemia/reperfusion.Scientific reports · 2015Article
- Article
- Catestatin increases the expression of anti-apoptotic and pro-angiogenetic factors in the post-ischemic hypertrophied heart of SHR.PloS one · 2014Article
- The surging role of Chromogranin A in cardiovascular homeostasis.Frontiers in chemistry · 2014Review
- Obligatory role for endothelial heparan sulphate proteoglycans and caveolae internalization in catestatin-dependent eNOS activation.BioMed research international · 2014Article
- Catestatin reduces myocardial ischaemia/reperfusion injury: involvement of PI3K/Akt, PKCs, mitochondrial KATP channels and ROS signalling.Pflugers Archiv : European journal of physiology · 2013Article
- The novel chromogranin A-derived serpinin and pyroglutaminated serpinin peptides are positive cardiac β-adrenergic-like inotropes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsCatestatin (CST) is a chromogranin A (CgA)-derived peptide (hCgA352-372) with three identified human variants (G364S/P370L/R374Q-CST) that show differential potencies towards the inhibition of catecholamine release. Although CST affects several cardiovascular parameters, the mechanisms underlying CST action in the heart have remained elusive. Therefore, we sought to determine the mechanism of action of CST and its variants on ventricular myocardium and endothelial cells. METHODS AND
resultsContractile force and Ca(2+) transients were measured, respectively, on rat papillary muscles and isolated cardiomyocytes (CC) under basal conditions and after β-adrenergic stimulation. Nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) phosphorylation (P(Ser1179)eNOS) were studied in bovine aortic endothelial (BAE-1) cells. Under basal conditions, wild-type CST (WT-CST, 10-50 nM) transiently enhanced myocardial contractility. CST variants (G364S and P370L) exerted a comparable positive inotropic effect. The H(1) histamine receptor antagonist mepyramine abolished the increase of contractile force induced by WT-CST. Moreover, WT-CST dose-dependently (5-50 nM) reduced the effect of β-adrenergic stimulation. This anti-adrenergic effect was not mediated by a direct action on CC, but involved a PI3K-dependent NO release from endocardial endothelial cells. Indeed, CST induced a wortmannin-sensitive, Ca(2+)-independent increase in NO production and eNOS phosphorylation on BAE-1 cells. While the anti-adrenergic and NO release effects of P370L-CST were comparable with those of WT-CST, the G364S variant was ineffective on the same parameters.
conclusionOur results suggest that the anti-adrenergic action of CST depends on the endothelial PI3K-Akt-eNOS pathway and that its structural alterations entail functional features that correlate with the different anti-hypertensive potential described in humans.
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